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PubMed1985

Pancreatic polypeptide in islet cell tumors. Morphologic and functional correlations.

Twelve islet cell tumors and one islet cell hyperplasia were studied with immunocytochemical and radioimmunoassay methods. With immunocytochemical staining, all six insulinomas, one mixed insulinoma-glucagonoma, and four gastrinomas were positive for insulin, insulin and glucagon, and gastrin, respectively. Pancreatic polypeptide (PP) was positive in three insulinomas and one mixed insulinoma-glucagonoma. All of the tumors were positive for neuron-specific enolase (NSE). Radioimmunoassays of tissue extracts further disclosed that all functioning tumors contained more than one pancreatic hormone. PP concentrations of two insulinomas and one mixed insulinoma-glucagonoma were higher than that of normal control pancreases. A study of protein meal-stimulated PP secretion revealed that three of the insulinoma cases and two gastrinoma cases exhibited higher plasma PP levels than the age-matched controls. The findings suggest that: both functioning and nonfunctioning islet cell tumors derive from neuroendocrine cells positive for NSE; all functioning islet cell tumors appear to contain PP in the tumor tissue as a minor component; as many as 70% of the patients with islet cell tumors present with abnormally higher plasma PP levels after protein meals; and a study of meal-stimulated PP secretion may well be used as a marker for the presence of functional islet cell tumors.

Adenoma, Islet Cell↗
PubMed1986

Cloned cell lines from a transplantable islet cell tumor are heterogeneous and express cholecystokinin in addition to islet hormones.

A liver metastasis (MSL) with a remarkable in vitro proliferation potential has been identified in an NEDH rat carrying a transplantable x-ray-induced islet cell tumor. Two insulin-secreting cell lines, MSL-G and MSL-H, with doubling times of 3-5 d were established by repeated limiting dilution cloning. In vivo inoculation of MSL-G cells induced severe hypoglycemia caused by a small but highly heterogeneous tumor as revealed by immunocytochemistry. Whereas most cells stained for the islet hormones, insulin, glucagon, and somatostatin, clustered cells were discovered to contain cholecystokinin (CCK). Additional in vitro-limiting dilution cloning, followed by immunocytochemical characterization, clearly demonstrated the capacity of single cell clones to simultaneously express the same four hormones. Radioimmunoassays with a panel of site-specific antisera of culture supernatants and purified cell extracts showed the MSL-G2 cells to produce, store, and secrete readily detectable amounts of processed and unprocessed CCK. Gastrin was not detected while coexpression of glucagon and CCK were demonstrated. Mutant clones selected for resistance to 6-thioguanine (frequency, 2 X 10(-7] and checked for HAT (hypoxanthine, aminopterin, thymidine) sensitivity retained the capacity for multi-hormone expression. We propose that the MSL tumor contains pluripotent endocrine stem cells. The MSL tumor and the MSL-G2 cells in particular will allow studies of not only CCK biosynthesis and processing but also of mechanisms involved in tumor and islet cell differentiation.

Adenoma, Islet Cell↗
PubMed2000

Metabolism of D-[1,2-13C]glucose and alpha-D-[1,2-13C]glucose pentaacetate in tumoral pancreatic islet cells.

Tumoral pancreatic islet cells of the RINm5F line were incubated, in groups of 25x106 cells each, for 120 min at 37 degrees C in media (5. 0 ml) containing either alpha-D-[1,2-13C]glucose pentaacetate (1.7 mM) or both D-[1,2-13C]glucose (1.7 mM) and acetate (8.5 mM). In both cases, the amounts of 13C-enriched metabolites (D-glucose, L-lactate and acetate) and non-enriched metabolites (acetate) recovered in the incubation medium after incubation were close to the initial amount of esterified or non-esterified D-[1, 2-13C]glucose and acetate, respectively. The 13C-enriched metabolites corresponded mainly to double-labelled D-[1, 2-13C]glucose, L-[2,3-13C]lactate and [1,2-13C]acetate. The output of L-[2,3-13C]lactate and [1,2-13C]acetate was about 3-4 times lower in the cells exposed to alpha-D-[1,2-13C]glucose pentaacetate than in those incubated with unesterified D-[1,2-13C]glucose. These findings indicate that, despite extensive hydrolysis of alpha-D-[1, 2-13C]glucose pentaacetate in the RINm5F cells, the hexose moiety of the ester is less efficiently metabolized than unesterified D-[1, 2-13C]glucose tested at the same molar concentration (1.7 mM) in the presence of 8.5 mM acetate. Thus, a higher utilization of the hexose moiety of alpha-D-glucose pentaacetate than that of unesterified D-glucose, as previously documented in isolated pancreatic islets, represents a far-from-universal situation.

Acetates↗
PubMedDate not supplied

Islet cell tumor.

A case of islet cell tumor occurring in a patient with the multiple endocrine neoplasia type I syndrome is reported. Immunostaining for insulin was strongly positive in the tumor cells. Numerous dense-core granules of endocrine caliber were identified ultrastructurally. Morphometric analysis of the secretory granules in 20 islet cell tumors gave a granule size of 182 +/- 52 nm (mean +/- standard deviation).

Adenoma, Islet Cell↗
PubMed2000

Acinar-islet cell tumor of the pancreas: report of a malignant pancreatic composite tumor.

An unusual case of malignant pancreatic composite tumor with both components of acinar cell tumor (ACT) and islet cell tumor (ICT) was investigated histologically, immunohistochemically, and ultrastructurally. The pancreatic tumor with central cyst formation was found on computerized tomographic examination of a 72-year-old man reporting appetite and weight loss. The ACT component was present in the original pancreatic region and the ICT region was adjacent to the ACT. ACT was immunohistochemically positive for pancreatic amylase, whereas ICT had argyrophil tumor cells immunohistochemically positive for chromogranin A. There were several tumor cell nests positive for both pancreatic amylase (acinar differentiation) and chromogranin A (islet differentiation). We speculated that ICT may have arisen from the de-differentiated tumor cells in the ACT after the occurrence of ACT.

Aged↗
PubMed1983

Computed tomography and nuclear magnetic resonance imaging of pancreatic islet cell tumors.

Eleven patients with pancreatic islet cell tumors smaller than 2.5 cm were examined by use of computed tomography (CT) and new scanning protocol. Seven of 11 tumors were localized and CT accurately assessed multiple lesions, retroperitoneal invasion, or liver metastases when present. CT is now the initial imaging procedure of choice for diagnosis and staging of islet cell tumors. Nuclear magnetic resonance can distinguish islet cell tumors from normal retroperitoneal structures and appears to be a promising new pancreatic imaging modality.

Adenoma, Islet Cell↗
PubMed1999

Immunocytochemical Localization of Glucose Transporter-2 (GLUT-2) in Pancreatic Islets and Islet Cell Tumors.

Glucose is a major metabolic fuel in mammals and is transported into organs and cells by a facilitated diffusion which involves binding of glucose to glucose transporters (GLUTs). Among several GLUTs so far indentified, GLUT-2 is specifically localized immunocytochemV cally in beta-islet cells. Using immunocytochemical staining, normal pancreases and 27 cases of islet cell tumors, including insulinomas, gastrinomas, glucagonomas, pancreatic polypeptide-omas (PPomas), and a nonfunctioning islet cells tumor, were systematically stained for four different pancreatic hormones, gastrin, and GLUT-2. GLUT-2 staining in beta-islet cells was more diffuse than that of insulin immunostaining, and corresponded with the positive staining in the lateral segments of beta-cell plasma membrane, that faced adjacent beta-cells. Glucagon, somatostatin (SRIF) and PP cells stained weakly for GLUT-2, weaker than that of beta-cells. Some nonbeta cells, especially extra-islet PP cells were not stained for GLUT-2. Among islet cell tumors, insulinomas stained less strongly for GLUT-2 than normal beta-cells from the adjacent normal pancreas. Gastrinomas, glucagonomas, and PPomas stained weaker than insulinomas. Even nonfunctioning islet cell tumors were weakly stained for GLUT-2. The positive staining for GLUT-2 observed for islets cells and all islet tumors is consistent with the notion that all pancreatic islet cells and islet cell tumors utilize glucose as a major fuel, requiring transporter-facilitated diffusion of glucose into the cells of normal organ and their tumors.

Journal Article↗
PubMed1995

Pleomorphic nonfunctioning islet cell tumor of the pancreas.

A nonfunctioning islet cell tumor of the pancreas in a 68-yr-old female is reported. All of the laboratory data, including serum hormones, glucose, and tumor markers, were within normal limits. A pancreatoduodenectomy was performed. Cut sections of the specimen revealed a cystic mass measuring 6.0 x 4.5 x 3.5 cm. Histologically, the tumor consisted of large acidophilic cells with bizarre giant nuclei. The tumor cells were positive for chromogranin-A, synaptophysin, neuron-specific enolase, and S-100 protein. Multifocal proliferation of endocrine cells, centroacinar cells and changes in acinar cells were found in the adjacent uninvolved pancreatic tissue. Ultrastructural studies of the tumor revealed clear nuclei with no zymogen, but immature neurosecretory granules in the cytoplasm of the tumor cells. These findings were consistent with those of nonfunctioning islet cell tumors, especially of the pleomorphic type. To the best of our knowledge, this is the first report on pleomorphic nonfunctioning pancreatic islet cell tumors.

Adenoma, Islet Cell↗
PubMed2000

[Treatment of malignant pancreatic islet cell tumors].

Among 142 patients with islet cell tumor who were admitted to hospital between 1982 and 1999, 15 patients (10.6%) had malignant tumours. The mean age was 45.3 +/- 5.8 years. Islet cell tumors were located in the head and corpus of the pancreas in 26.6% and 26.6% of the patients, respectively, in the tail of the pancreas in 46.8% of the patients. The mean size of the tumor was 2.9 +/- 0.7 cm, in 6 patients (40%) liver metastases were found. US, CT and angiography which sensitivity were 72.7, 100 and 85.7%, respectively, were used for topical diagnosis of the islet cell tumors. 12 patients were operated on (15 operations) and 3 patients were treated conservatively by streptozocin. Surgical procedures included distal pancreatic resection (n = 11), enucleation of the tumor (n = 2), hepatic resection (n = 1), abdominal exploration (n = 1). In 2 patients palliative pancreatic resections were combined with transarterial embolization and devascularisation of the liver metastases and 2 patients were treated by systemic chemotherapy. To reveal malignancy before and during the operation was possible only by evaluation of distant metastases and the adjacent organs infiltration. In other cases to determine the diagnosis was possible only after planned histological identification of the resected specimens. 5-year survival rates after conservative and surgical treatment were 33% and 62.5%, respectively. In patients without distant metastases 5-year survival rate was 100%.

Adult↗
PubMed1993

Functional islet cell tumor in six ferrets.

Functional islet cell tumor was diagnosed in 6 ferrets. Prominent clinical signs included weight loss, hind limb weakness, ptyalism, and tremors. The diagnosis was made on the basis of 2 or more of the following methods and confirmed by histologic examination of biopsied tissue: hypoglycemia on routine serum biochemical analysis, clinical signs of hypoglycemia, simultaneous development of hypoglycemia (44 +/- 9.9 mg/dl; mean +/- SD), and hyperinsulinemia (58 +/- 18.4 microU/ml; mean +/- SD) after food was withheld for 4 hours. Surgical resection of affected tissue was associated with clinical improvement in all cases. Foci of metastasis were found in 1 ferret. Diazoxide was unsuccessful in controlling persistent postsurgical hypoglycemia in 2 ferrets. Additional functional islet cell tumors were identified in 5 of 6 ferrets at necropsy. Functional islet cell tumors are important neoplasms of older ferrets. Preventive health programs for ferrets > 3 years old should include monthly weight determinations and biannual CBC and serum biochemical analysis.

Adenoma, Islet Cell↗
PubMed1999

Immunohistochemical localization of betacellulin, a new member of the EGF family, in normal human pancreas and islet tumor cells.

Betacellulin (BTC) purified from mouse beta cell tumor (betaTC-3) is a new member of the epidermal growth factor (EGF) family which can bind receptor tyrosine kinase, EGF receptor (erbB1) and erbB4. It has been demonstrated that proBTC mRNA was abundantly expressed in human pancreas tissue, and that BTC converted amylase-secreting rat acinar cell line (AR42J) into insulin-secreting cells, suggesting that BTC might be important for the growth and/or differentiation of islet cells. However, the cell type producing BTC in the pancreas has not been clarified. In this study, we examined the localization of BTC in human pancreas and islet cell tumors. Immunohistochemistry using specific antibodies to human BTC revealed that this protein was produced in alpha cells and duct cells, and probably in beta cells in normal adult pancreas. Furthermore, strong immunoreactivity to BTC was detected in primitive duct cells of the fetal pancreas, and both insulinoma and glucagonoma cells also showed positive immunoreactivity to BTC. EGF receptor (erbB1) and erbB4 were expressed mainly in islet and duct cells, and duct cells, respectively. These results demonstrate the localization of BTC and its receptors, and suggest that BTC may be one of the factors that have physiologically important roles such as growth and differentiation of islet cells in the human pancreas.

Adenoma, Islet Cell↗
PubMed2004

Natural history of a patient with malignant nonfunctioning islet cell tumor associated with unresectable multiple liver metastases.

Islet cell tumors of the pancreas are uncommon. Approximately 15% of islet cell tumors are nonfunctioning and have a higher malignancy rate than their functioning counterparts. Though, because of the rarity of malignant nonfunctioning islet cell tumors, the natural history of a patient with this tumor has not been clearly defined. We describe a young patient with unresectable malignant nonfunctioning islet cell tumor associated with multiple liver metastases. He was treated with palliative therapies to improve his quality of life, but did not undergo surgical removal of tumors or systemic chemotherapy. He survived for 46 months since laparotomy for histological diagnosis. Our findings may represent the natural history of patients with unresectable malignant nonfunctioning islet cell tumor, and suggest that palliative therapy may contribute not only to the improvement of a patients' quality of life but also the prolongation of survival.

Adult↗
PubMed1978

Biochemical studies on rats with insulin-secreting islet cell tumors induced by streptozotocin: with special reference to physiological response to oral glucose load in the course of and after tumor induction.

Pancreatic islet cell tumors were induced in 32 of 49 male Wistar rats (73%) surviving 9 months or longer following treatment with streptozotocin alone, with streptozotocin and nicotinamide, or with streptozotocin and picolinamide. Serial oral glucose tolerance tests in rats treated with streptozotocin and nicotinamide showed that the elevation of blood glucose levels after oral glucose load was depressed significantly 7 months after treatment. Plasma insulin responses were distinctly elevated 9 months after treatment. Blood glucose levels remained lower and plasma insulin levels rose markedly after a glucose load in tumor-bearing rats as compared to the response of tumor-free rats. These findings suggest that pancreatic islet cell tumors induced by streptozotocin with and without combined treatment are insulin-secreting, and that streptozotocin itself has oncogenic effects on the rat pancreas. Mean insulin concentration in islet cell tumors amounted to 401 U/g wet wt, whereas the concentration was 14 U/g wet wt in the pancreatic tissue from tumor-free rats.

Adenoma, Islet Cell↗
PubMed2004

Non-islet origin of pancreatic islet cell tumors.

The histogenesis of pancreatic islet cell tumors was investigated by morphological identification of putative precursor lesions in pancreatic tissue from patients with multiple endocrine neoplasia type 1 (MEN1), tissue microdissection, and genetic analysis. MEN1 mutation and absence of the MEN1 wild-type allele in different precursor lesions strongly suggest that pancreatic islet cell tumors are derived from the ductal/acinar system but not from pancreatic islet tissue. Pluripotent cells within the exocrine pancreas appear capable of formation into small atypical accumulations of MEN1-deficient cells with both exocrine and endocrine phenotype. The findings suggest presence of multiple developmental aberrations in MEN1 pancreas that potentially serve as precursor material for neuroendocrine tumors.

Adenoma, Islet Cell↗
PubMed1994

Islet cell tumors of the pancreas.

Islet cell tumors of the pancreas are present in 65% to 80% of patients with MEN 1 syndrome. The tumors are typically multifocal and may secrete multiple peptides either concurrently or at different times in the course of a patient's disease. Gastrinomas are most common and present the Zollinger-Ellison syndrome. Although curative surgery is possible in some cases, medical therapy is quite effective in most. Hypoglycemia due to insulin-secreting tumor is amenable to curative surgery in many cases. With prospective family screening programs and improved diagnostic techniques the disease is being diagnosed at an early, often preclinical stage in recent years.

Carcinoma, Islet Cell↗
PubMed1989

Systemic and regional therapy of advanced islet cell tumors.

Asymptomatic patients with islet cell tumors should be observed every 3 to 6 months. Once symptomatic, many therapeutic choices exist. First choice would be symptomatic management resulting in minimum side effects. More aggressive approaches include systemic therapy with cytotoxic or biologic agents. Vascular occlusion provides useful palliation of liver metastases.

Adenoma, Islet Cell↗